Hippocampal Deficits in Amyloid-β-Related Rodent Models of Alzheimer’s Disease
Front. Neurosci.. 2020-04-07; 14:
DOI: 10.3389/fnins.2020.00266
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Vyas Y(1), Montgomery JM(1), Cheyne JE(1).
Author information:
(1)Department of Physiology, Centre for Brain Research, University of Auckland,
Auckland, New Zealand.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease that is the
most common cause of dementia. Symptoms of AD include memory loss,
disorientation, mood and behavior changes, confusion, unfounded suspicions, and
eventually, difficulty speaking, swallowing, and walking. These symptoms are
caused by neuronal degeneration and cell loss that begins in the hippocampus, and
later in disease progression spreading to the rest of the brain. While there are
some medications that alleviate initial symptoms, there are currently no
treatments that stop disease progression. Hippocampal deficits in
amyloid-β-related rodent models of AD have revealed synaptic, behavioral and
circuit-level defects. These changes in synaptic function, plasticity, neuronal
excitability, brain connectivity, and excitation/inhibition imbalance all have
profound effects on circuit function, which in turn could exacerbate disease
progression. Despite, the wealth of studies on AD pathology we don’t yet have a
complete understanding of hippocampal deficits in AD. With the increasing
development of in vivo recording techniques in awake and freely moving animals,
future studies will extend our current knowledge of the mechanisms underpinning
how hippocampal function is altered in AD, and aid in progression of treatment
strategies that prevent and/or delay AD symptoms.
Copyright © 2020 Vyas, Montgomery and Cheyne.